Cardiac Arrhythmias Flashcards by Rosie Ellis

Define arrhythmias

Any variation from the normal rate of rhythm of heart beat

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What can the classification of cardiac arrhythmias be based on?

Rate

Site of origin

Mechanism

ECG appearance

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Describe the phases of cardiac pacemaker cell action potentials

Phase 0: Ca2+ in

Phase 3: K+ out

Phase 4: Na+ in, Ca2+ in

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Describe the phases of cardiac muscle cell action potentials

Phase 0: Rapid Na⁺ influx through open fast Na⁺ channels
Phase 1: Transient K⁺ channels open; K⁺ efflux returns TMV to 0mV.
Phase 2: Influx of Ca²⁺ through L-type Ca²⁺ channels is electrically balanced by K⁺ efflux through delayed rectifier K⁺ channels.
Phase 3: Ca²⁺ channels close, delayed rectifier K⁺channels remain open and return TMV to -90mV
Phase 4: Na⁺, Ca²⁺ channels closed. OPen K⁺ rectifier channels keep TMV stable at -90mV.

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Describe normal sinus rhythm

Rate: 60-100bpm
Rhythm: regular
P waves: present and preceding each QRS complex
PR interval: normal (0.12-0.2 secs)
QRS: Normal (<0.12 secs)

Rate and rhythm may vary with respiration (increases on inspiration; decreases on expiration)

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What are the 2 main mechanisms of cardiac arrhythmias?

Name examples of each

Altered impulse formation

Increased automaticity
Decreased automaticity

Altered impulse conduction

Conduction block
Re-entry

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What are the cardiac causes of bradycardia?

Age-related degeneration/fibrosis
Infection
Ischaemia
Cardiomyopathy
Congenital

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Name some systemic causes of bradycardias

Drugs
Hypothermia
Hypothyroidism
Electrolyte abnormalities
Autonomic dysfunction

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Describe sinus bradycardia

Rate: <60bpm
Rhythm: regular
QRS, P wave, PR interval all normal

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Describe sinus pause/arrest

Rate: can be normal/slow
Rhythm: irregular due to pause
P wave, PR interval and QRS all normal

Caused by failure of SA node to fire, therefore the next P wave does not occur at the expected time

Escape rhythms from latent pacemakers may occur during pause

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Describe first degree heart block

Delayed AV conduction = prolonged PR interval

Often asymptomatic

Rate: usually <60bpm
Rhythm: regular
Usually asymptomatic, no treatment required
Normal P wave and QRS complex
PR interval prolonged due to delayed conduction
No missed beats

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Describe second degree heart block type 1

Rate: Usually <60bpm
Rhythm: irregular
P wave: present but more P waves than QRS
PR interval: progressively prolonged until beat drops
QRS normal

Intermittent failure of conduction; PR interval ‘resets’ after each dropped beat and cycle restarts- Wenckenbach phenomenon (Mobitz type 1)

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Describe second degree heart block type 2

Rate: usually <60bpm
Rhythm: irregular
P wave: present but more P waves than QRS
PR interval: normal or prolonged
QRS: may be normal or prolonged

Intermittent failure of conduction; constant PR interval.

Can cause palpitations, dizziness, syncope, chest pain, confusion through haemodynamic compromise.

Admit for monitoring, investigate possible ischaemia

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Descrive third degree (complete) heart block

Rate: atrial rate higher than slow ventricular rate (escape rhythm)
Rhythm: regular
P wave: more P waves than QRS, no clear relationship
PR interval: absent (AV dissociation)
QRS: normal or broad depending on site of ventricular escape rhythm

Complete failure of conduction; P waves and QRS completely unrelated

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How should third degree heart block be managed?

Cardiac monitoring
Atropine
Pacing: transcutaneous/temp pacing wire/ PPM

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Name some causes of tachycardias

Anxiety
Drugs
Alcohol
Hyperthyroidism
Hypoxaemia
Ischaemia
Hypotension
Electrolyte abnormalities
Infection
Cardiomyopathy
Fibrosis

What are the 2 main classifications of tachycardias?

Supraventricular (arising above the ventricles)
Ventricular (arising within the ventricles)

Name types of supraventricular tachycardias

Sinus tachycardia
Paroxysmal/ re-entrant SVTs
- Atrioventricular nodal re-entrant tachycardia
- Atrioventricular re-entrant (reciprocating) tachycardia
Atrial flutter
Atrial fibrillation

Name types of ventricular tachycardias

Premature ventricular complex
Ventricular tachycardia
Ventricular fibrillation

Describe sinus tachycardia

Rate: 100-180bpm
Rhythm: regular
P waves: present and preceding each QRS
PR interval: normal
QRS: normal

Usually an appropriate response to an underlying condition

Describe paroxysmal/ re-entrant SVTs

Rate: 140-280bpm
Rhythm: normal
P waves merged with QRS- retrograde conduction
PR interval usually not seen
QRS normal

Usually due to re-entry circuit within AV node (AVRNT)- activates both atria and ventricles

May be caused by re-entry circuit using AV node and accessory pathway

Describe pre-excitation

Rate: Normal
Rhythm: regular
P wave: present and precedes each QRS
PR interval: may be short
QRS: often broad due to delta wave

= Early activation of the ventricles as impulses bypass AV node via accessory pathway.

Short PR interval and slurring into QRS complex (delta wave)

May give rise to AVRT

Symptomatic patients: Wolff-Parkinson-White syndrome

Describe atrial flutter

Ventricular rate depends on rate of AVN
Rhythm: typically regular
P wave not seen- flutter ‘F’ waves
PR interval not measurable
QRS normal
Re-entry circuit within atria

Describe atrial fibrillation

Rate: depends on rate of AVN
P wave absent
Irregular rhythm (intermittent conduction through AVN)
Absent PR interval
QRS usually normal

Uncoordinated atrial activity: fibrillating waves rather than P waves.

Thromboembolism risk

May be paroxysmal, acute, persistent or permanent

Describe Torsade de Pointes

* Fast (200-250 bpm) * Irregular rhythm * P wave not visible * Broad QRS * Specific form of polymorphic VT, prolonged QT interval

Describe premature ventricular complex

* Underlying rate * Irregular rhythm * P wave absent during PVC * PR interval not measurable during PVC * Broad QRS, abnormal morphology Spontaneous early discharge from ectopic pacemaker in ventricle

Describe ventricular tachycardia

* Fast rate (100-250 bpm) * Regular rhythm * No P wave * PR interval not measurable * Broad QRS * May impair cardiac output (pulseless VT) * Can be monomorphic (most common) or polymorphic

Describe ventricular fibrillation

* Rate often unmeasurable * Irregular rhythm * Absent P wave * PR interval absent * QRS: no organised ventricular activity Rapid uncoordinated irregular ventricular contractions Incompatible with adequate cardiac output / pulseless

What is automaticity?

The property of spontaneous depolarisation, usually only in the SAN, AV and conducting tissues of the heart.

What is enhanced automaticity? What are the 2 types?

Other myocardial cells exhibiting automaticity potentially leading to spontaneous depolarisation at sites other than the SAN giving rise to ectopic beats and tachycardias. **Enhanced normal automaticity:** accelerated generation of an action potential by normal pacemaker tissue. **Abnormal automaticity:** accelerated generation of an action potential by abnormal tissue within the myocardium.

Which factors may enhance automaticity? How do these factors cause enhanced automaticity?

* Catecholamine excess * Ischaemia * Abnormal pH * Electrolyte abnormalities Enhanced automaticity may be caused by factors that decrease the threshold or increase the slope of phase 4 depolarisation.

What is triggered activity?

Triggered activity results from the premature activation of cardiac tissues by afterdepolarisations, which are depolarizations triggered by one or more preceding action potentials. These afterdepolarisations can be early (before full repolarisation- phase 2-3) or delayed (after full repolarisation- phase 4 of the cardiac cycle). The new AP generated can then generate another AP leading to sustained triggered activity.

What is re-entry? How does it differ from normal conduction? What types of arrhythmias does re-entry underlie?

Normal conduction usually results in uniform spread of depolarisation in a constant direction. Re-entry occurs when the depolarisation wave is able to form a self-propagating looped circuit. Underlies tachycardias including: * Atrial flutter * Re-entrant tachycardias (AVNRT and AVRT * Some ventricular tachycardias

What are the pre-requisites for 'classic' re-entry to occur?

* At least two pathways or the presence of a barrier along the conduction pathway * Unidirectional block in one of the pathways * Conduction must be slow enough (and/or refractory period short enough) to prevent the depolarisation wave encountering refractory tissue within the circuit

What is occuring in these images of re-entry?

In (1) the impulse passes down both limbs of the potential tachycardia circuit (normal conduction). In (2) the impulse is blocked in one pathway (α) (e.g. still in refractory phase), but proceeds slowly down pathway β, returning along pathway α until it collides with refractory tissue. In (3) the impulse travels so slowly along pathway β that it can return along pathway α and complete the re-entry circuit, producing a circus movement tachycardia.